Evidence map›Paper›PMID 36032168›Full record

ArticleFrontiers in immunology2022

Phenotypic and functional analysis of γδ T cells in the pathogenesis of human T-cell lymphotropic virus type 1 infection.

Matias Ruggieri, Nicolás Ducasa, Claudia Juraske, Virginia Gonzalez Polo, Carolina Berini, Maria Florencia Quiroga, Petros Christopoulos, Susana Minguet, Mirna Biglione, Wolfgang W Schamel

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 60% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 1 citations in OpenAlex.

  1. Review
  2. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 2 countries.

Matias RuggieriDepartment of Immunology, Faculty of Biology, Albert-Ludwigs-University of Freiburg, Freiburg, Germany.
Nicolás DucasaNational Scientific and Technical Research Council (CONICET), University of Buenos Aires, Institute for Biomedical Research in Retroviruses and AIDS (INBIRS), Buenos Aires, Argentina.
Claudia JuraskeDepartment of Immunology, Faculty of Biology, Albert-Ludwigs-University of Freiburg, Freiburg, Germany.
Virginia Gonzalez PoloNational Scientific and Technical Research Council (CONICET), University of Buenos Aires, Institute for Biomedical Research in Retroviruses and AIDS (INBIRS), Buenos Aires, Argentina.
Carolina BeriniNational Scientific and Technical Research Council (CONICET), University of Buenos Aires, Institute for Biomedical Research in Retroviruses and AIDS (INBIRS), Buenos Aires, Argentina.
Maria Florencia QuirogaNational Scientific and Technical Research Council (CONICET), University of Buenos Aires, Institute for Biomedical Research in Retroviruses and AIDS (INBIRS), Buenos Aires, Argentina.
Petros ChristopoulosDepartment of Thoracic Oncology, Thoracic Clinic at Heidelberg University Hospital, Heidelberg, Germany.
Susana MinguetDepartment of Immunology, Faculty of Biology, Albert-Ludwigs-University of Freiburg, Freiburg, Germany.
Mirna BiglioneNational Scientific and Technical Research Council (CONICET), University of Buenos Aires, Institute for Biomedical Research in Retroviruses and AIDS (INBIRS), Buenos Aires, Argentina.
Wolfgang W SchamelDepartment of Immunology, Faculty of Biology, Albert-Ludwigs-University of Freiburg, Freiburg, Germany.
Instituto de Investigaciones Biomédicas en Retrovirus y Sida · ARConsejo Nacional de Investigaciones Científicas y Técnicas · ARUniversity Medical Center Freiburg · DEUniversity of Freiburg · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human T-cell leukemia virus type 1 (HTLV-1) is the cause of serious malignant and inflammatory diseases, including adult T-cell leukemia and lymphoma and tropical spastic paraparesis. The potential protective role of γδ T cells in HTLV-1 infection remains unclear. Here, demonstrate that there is a decrease in the amount of Vγ9Vδ2 T cells in patients with HTLV-1, especially in those with HTLV-1 associated pathologies. This suggests that γδ T cells could be involved in controlling the virus. Indeed, we found that Vγ9Vδ2 T cells, expanded from non-infected individuals, can kill cells expressing the viral proteins HBZ and Tax and this phenotype is reversed in the presence of mevastatin. Cytotoxicity by Vγ9Vδ2 T cells was not associated with an increase of INF-γ production. In sharp contrast, killing by NK cells was reduced by Tax expression. Thus, our study provides initial evidence for a potential protective role of Vγ9Vδ2 T cells against HTLV-1 infection. Therapeutic exploitation of these insights is feasible with current technologies of T-cell therapies and could provide novel tools to prevent and treat HTLV-1-associated malignancies and neurologic complications.

Indexed as

HTLV-I InfectionsHuman T-lymphotropic virus 1Paraparesis, Tropical SpasticAdultHumansPhenotypeT-LymphocytescytotoxicityHTLV-1IFN-γmevalonate pathwayγδ T cells

Identifiers

PMID36032168
PMCPMC9403740
OpenAlexW4291016612

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.